Current Issue : January - March Volume : 2015 Issue Number : 1 Articles : 7 Articles
Background: Patients with end-stage renal disease (ESRD) have multiple comorbid conditions. Obtaining comorbidity\ndata from medical records is cumbersome. A self-report comorbidity questionnaire is a useful alternative. Our aim in this\nstudy was to examine the predictive value of a self-report comorbidity questionnaire in terms of survival in ESRD patients.\nMethods: We studied a prospective cross-sectional cohort of 282 haemodialysis (HD) patients in a single centre.\nParticipants were administered the self-report questionnaire during an HD session. Information on their comorbidities was\nsubsequently obtained from an examination of the patientââ?¬â?¢s medical records. Levels of agreement between parameters\nderived from the questionnaire, and from the medical records, were examined. Participants were followed-up for 18\nmonths to collect survival data. The influence on survival of comorbidity scores derived from the self-report data\n(the Composite Self-report Comorbidity Score [CSCS]) and from medical records data - the Charlson Comorbidity Index\n[CCI] were compared.\nResults: The level of agreement between the self-report items and those obtained from medical records was almost\nperfect with respect the presence of diabetes (Kappa score ? 0.97), substantial for heart disease and cancer (? 0.62 and\n? 0.72 respectively), moderate for liver disease (? 0.51), only fair for lung disease, arthritis, cerebrovascular disease, and\ndepression (? 0.34, 0.35, 0.34 and 0.29 respectively). The CSCS was strongly predictive of survival in regression models\n(Nagelkerke R2 value 0.202), with a predictive power similar to that of the CCI (Nagelkerke R2 value 0.211). The influences\nof these two parameters were additive in the models ââ?¬â?? suggesting that these parameters make different contributions\nto the assessment of comorbidity.\nConclusion: This self-report comorbidity questionnaire is a viable tool to collect comorbidity data and may have a role in\nthe prediction of short-term survival in patients with end-stage renal disease on haemodialysis. Further work is required in\nthis setting to refine the tool and define its role....
Background: Poor sleep quality, a novel risk factor of cardiovascular diseases (CVD), is highly prevalent in patients\nwith chronic kidney disease (CKD). The association between poor sleep quality and cardiovascular damage in\npatients with CKD is unclear. This study is aimed to assess the prevalence and related risk factors of sleep\ndisturbance and determine the relationship between sleep quality and cardiovascular damage in Chinese patients\nwith pre-dialysis CKD.\nMethods: A total of 427 pre-dialysis CKD patients (mean age = 39 �± 15 years, 260 male/167 female) were recruited\nin this study. The demographics and clinical correlates were collected. The sleep quality was measured by the\nPittsburgh Sleep Quality Index (PSQI), whereas the cardiovascular damage indicators (the Early/late diastolic\npeak flow velocity (E/A) ratio and left ventricular mass index (LVMI)) were determined by an echocardiographic\nexamination.\nResults: Of the CKD patients, 77.8% were poor sleepers as defined by a PSQI score > 5. Median estimated\nglomerular filtration rate (eGFR) was 69.4(15.8-110.9) ml/min/1.73 m2. Logistic regression analysis revealed that left\nventricular hypertrophy (LVH) was independently associated with the PSQI score (OR = 1.092, 95% CI = 1.011-1.179,\np = 0.025), after adjustment for age, sex and clinical systolic blood pressure, diastolic blood pressure, Phosphate,\nIntact parathyroid hormone (iPTH), Hemoglobin and eGFR. The linear regression analysis showed that the E/A ratios\nwere independently associated with the PSQI score (? = ?0.115, P = 0.028) after adjustment for a series of potential\nconfounding factors.\nConclusions: Poor sleep quality, which is commonly found in pre-dialysis CKD patients, is an independent factor\nassociated with cardiovascular damage in CKD patients. Our finding implies that the association between poor sleep\nand CVD might be mediated by cardiac remodeling....
Background: Expression and/or excretion of fibroblast growth factor-23 (FGF23) and its co-receptor Klotho are\naltered in patients with end-stage renal disease. The possibility that the FGF23/?-Klotho system mediates the\naggravated cardiovascular outcome among patients with chronic kidney disease (CKD) has been suggested. We\ndetermined whether FGF23 and ?-Klotho concentrations are altered among patients with reduced renal function\nand proteinuria.\nMethods: Serum FGF23 and ?-Klotho were measured in cardiology patients who were not undergoing chronic\nhemodialysis. Estimated glomerular filtration rate (eGFR) was correlated negatively with FGF23 and positively with\n?-Klotho.\nResults: The correlation between FGF23 and the renal tubular maximum reabsorption rate of phosphate to the\nGFR (TmP/GFR) was not significant, but that between FGF23 and serum calcium or inorganic phosphate was\nsignificant among patients with an estimated GFR of less than 60 mL/min/m2. By stepwise multivariate regression\nanalysis, eGFR was selected as significant predictor for FGF23 or ?-Klotho among patients with an estimated GFR of\nless than 60 mL/min/m2; however, urine albumin/creatinine ratio was not selected as a predictor for FGF23 or\n?-Klotho irrespective of the eGFR levels. In patients with eGFR of <60 mL/min/1.73 m2, UACR was significantly\nassociated with log(FGF23); but, this association did not remain statistically significant in a multivariate model.\nConclusions: Among cardiology patients with various stages of CKD, serum concentrations of FGF23 and ?-Klotho\nwere associated with renal function, but not with the extent of proteinuria....
Background: Diet can markedly affect acid-base status and it significantly influences chronic kidney disease (CKD)\nand its progression. The relationship of dietary acid load (DAL) and CKD has not been assessed on a population\nlevel. We examined the association of estimated net acid excretion (NAEes) with CKD; and socio-demographic and\nclinical correlates of NAEes.\nMethods: Among 12,293 U.S. adult participants aged >20 years in the National Health and Nutrition Examination\nSurvey 1999ââ?¬â??2004, we assessed dietary acid by estimating NAEes from nutrient intake and body surface area; kidney\ndamage by albuminuria; and kidney dysfunction by eGFR < 60 ml/min/1.73m2 using the MDRD equation. We\ntested the association of NAEes with participant characteristics using median regression; while for albuminuria, eGFR,\nand stages of CKD we used logistic regression.\nResults: Median regression results (? per quintile) indicated that adults aged 40ââ?¬â??60 years (? [95% CI] = 3.1 [0.3ââ?¬â??5.8]),\npoverty (? [95% CI] = 7.1 [4.01ââ?¬â??10.22]), black race (? [95% CI] = 13.8 [10.8ââ?¬â??16.8]), and male sex (? [95% CI] = 3.0 [0.7- 5.2])\nwere significantly associated with an increasing level of NAEes. Higher levels of NAEes compared with lower levels were\nassociated with greater odds of albuminuria (OR [95% CI] = 1.57 [1.20ââ?¬â??2.05]). We observed a trend toward greater NAEes\nbeing associated with higher risk of low eGFR, which persisted after adjustment for confounders.\nConclusion: Higher NAEes is associated with albuminuria and low eGFR, and socio-demographic risk factors for CKD are\nassociated with higher levels of NAEes. DAL may be an important target for future interventions in populations at high risk\nfor CKD....
Background: Hyperuricemia has been reported to be associated with chronic kidney disease (CKD). However\nwhether an elevated serum uric acid level is an independent risk factor for new-onset CKD remained controversial.\nMethods: A systematic review and meta-analysis using a literature search of online databases including PubMed,\nEmbase, Ovid and ISI Web/Web of Science was conducted. Summary adjusted odds ratios with corresponding 95%\nconfidence intervals (95% CI) were calculated to evaluate the risk estimates of hyperuricemia for new-onset CKD.\nResults: Thirteen studies containing 190,718 participants were included. A significant positive association was found\nbetween elevated serum uric acid levels and new-onset CKD at follow-up (summary OR, 1.15; 95% CI, 1.05ââ?¬â??1.25).\nHyperuricemia was found be an independent predictor for the development of newly diagnosed CKD in non-CKD\npatients (summary OR, 2.35; 95% CI, 1.59ââ?¬â??3.46). This association increased with increasing length of follow-up. No\nsignificant differences were found for risk estimates of the associations between elevated serum uric acid levels and\ndeveloping CKD between males and females.\nConclusions: With long-term follow-up of non-CKD individuals, elevated serum uric acid levels showed an\nincreased risk for the development of chronic renal dysfunction....
Background: Socioeconomic status (SES) is independently associated with chronic kidney disease (CKD)\nprogression; however, its association with other CKD outcomes is unclear. In particular, the potential differential\neffect of SES on mortality among blacks and whites is understudied in CKD. We aimed to examine survival among\nindividuals with prevalent CKD by income and race in the Reasons for Geographic and Racial Differences in Stroke\n(REGARDS) study.\nMethods: We examined 2,761 participants with prevalent CKD stage 3 or 4 between 2003 and 2007 in the\nREGARDS cohort. Participants were followed through March 2013. Mortality from any cause was assessed by\nincome and race (black or white). Low income was defined as an annual household income < $20,000, and was\ncompared to higher incomes (?$20,000). Cox proportional hazards models adjusted for age, gender, education,\ninsurance, CKD stage, comorbidity and county-level poverty were used to estimate hazard ratios (HR) and 95%\nconfidence intervals (CI).\nResults: A total of 750 deaths (27.5%) occurred during the follow-up period. Average follow-up time was 6.6 years\namong those alive and 3.7 years among those who died. Low income participants had an elevated adjusted hazard\nof mortality (HR = 1.58, 95% CI 1.24-2.00) compared to higher income participants. Low income was associated with\nall-cause mortality regardless of race (HR 1.53; 95% CI 1.18-1.99 among blacks and HR 1.38; 95% CI 1.10-1.74 among\nwhites), with no significant statistical interaction between household income and race (p-value = 0.634). However,\nblack participants had a higher adjusted hazard of mortality (HR = 1.30, 95% CI 1.02-1.65) compared to whites, which\nwas independent of income.\nConclusion: Income was associated with increased mortality for both blacks and whites with CKD. Blacks with CKD\nhad higher mortality than whites even after adjusting for important socio-demographic and clinical factors...
Background: A translational study in renal transplantation suggested YKL-40, a chitinase 3-like-1 gene product,\nplays an important role in acute kidney injury (AKI) and repair, but data are lacking about this protein in urine from\nnative human kidneys.\nMethods: This is an ancillary study to a single-center, prospective observational cohort of patients with\nclinically-defined AKI according to AKI Network serum creatinine criteria. We determined the association of\nYKL ?40 ? 5 ng/ml, alone or combined with neutrophil gelatinase-associated lipocalin (NGAL), in urine collected\non the first day of AKI with a clinically important composite outcome (progression to higher AKI stage and/or\nin-hospital death).\nResults: YKL-40 was detectable in all 249 patients, but urinary concentrations were considerably lower than in\npreviously measured deceased-donor kidney transplant recipients. Seventy-two patients (29%) progressed or died\nin-hospital, and YKL-40 ? 5 ng/ml had an adjusted odds ratio (95% confidence interval) for the outcome of 3.4\n(1.5-7.7). The addition of YKL-40 to a clinical model for predicting the outcome resulted in a continuous net\nreclassification improvement of 29% (P = 0.04). In patients at high risk for the outcome based on NGAL concentrations\nin the upper quartile, YKL-40 further partitioned the cohort into moderate-risk and very high-risk groups.\nConclusions: Urine YKL-40 is associated with AKI progression and/or death in hospitalized patients and improves\nclinically determined risk reclassification. Combining YKL-40 with other AKI biomarkers like NGAL may further delineate\nprogression risk, though additional studies are needed to determine whether YKL-40 has general applicability and to\ndefine its association with longer-term outcomes in AKI....
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